Evidence map›Paper›PMID 36017090›Full record

ArticleFrontiers in cardiovascular medicine2022

Empagliflozin prevents neointima formation by impairing smooth muscle cell proliferation and accelerating endothelial regeneration.

Jochen Dutzmann, Lena Marie Bode, Katrin Kalies, Laura Korte, Kai Knöpp, Frederik Julius Kloss, Mirja Sirisko, Claudia Pilowski, Susanne Koch, Heiko Schenk and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Jochen DutzmannMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Lena Marie BodeDepartment of Cardiology and Angiology, Hannover Medical School, Hanover, Germany.
Katrin KaliesMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Laura KorteDepartment of Cardiology and Angiology, Hannover Medical School, Hanover, Germany.
Kai KnöppMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Frederik Julius KlossDepartment of Cardiology and Angiology, Hannover Medical School, Hanover, Germany.
Mirja SiriskoDepartment of Cardiology and Angiology, Hannover Medical School, Hanover, Germany.
Claudia PilowskiMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Susanne KochMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Heiko SchenkDepartment of Nephrology and Hypertension, Hannover Medical School, Hanover, Germany.
Jan-Marcus DanielMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Johann BauersachsDepartment of Cardiology and Angiology, Hannover Medical School, Hanover, Germany.
Daniel G SeddingMid-German Heart Center, Division of Cardiology, Angiology and Intensive Medical Care, University Hospital Halle, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Martin Luther University Halle-Wittenberg · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Empagliflozin, an inhibitor of the sodium glucose co-transporter 2 (SGLT2) and developed as an anti-diabetic agent exerts additional beneficial effects on heart failure outcomes. However, the effect of empagliflozin on vascular cell function and vascular remodeling processes remains largely elusive. Methods/Results: Immunocytochemistry and immunoblotting revealed SGLT2 to be expressed in human smooth muscle (SMC) and endothelial cells (EC) as well as in murine femoral arteries. Conclusion: Empagliflozin significantly reduces serum-induced proliferation and migration of SMCs

Indexed as

diabetesneointima formationrestenosisSGLT2vascular remodeling

Identifiers

PMID36017090
PMCPMC9396257
OpenAlexW4290744544

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.